Retraction Note: TET2 inhibits tumorigenesis of breast cancer cells by regulating caspase-4

Zhu, Xuguo; Li, Shuangqi

doi:10.1038/s41598-019-39690-5

Cited by 14 publications

(17 citation statements)

References 26 publications

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“…It is most frequently mutated in several solid malignancies and is closely correlated with DNA methylation . Zhu et al reported that TET2 inhibited tumorigenesis of MCF‐7 cells by regulating caspase‐4 . Chen et al found that TET2 was frequently downregulated in glioma and that ectopic expression of TET2 inhibited the invasion and proliferation of glioma cells .…”

Section: Discussionmentioning

confidence: 99%

“…31 Zhu et al reported that TET2 inhibited tumorigenesis of MCF-7 cells by regulating caspase-4. 32 Chen et al found that TET2 was frequently downregulated in glioma and that ectopic expression of TET2 inhibited the invasion and proliferation of glioma cells. 33 In the present study, we found that the expression of TET2 was most significantly changed after miR-19a-5p knockdown in GBM cells.…”

Section: Ac0164053 Suppressed Tet2-mediated Proliferation and Metamentioning

confidence: 99%

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AC016405.3, a novel long noncoding RNA, acts as a tumor suppressor through modulation of TET2 by microRNA‐19a‐5p sponging in glioblastoma

Ren

2019

Cancer Science

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Long non‐coding RNAs (lncRNAs) are crucial regulators in various malignancies including glioblastoma multiforme (GBM). In the present study, we screened out a new lncRNA, AC016405.3, through a previous genome‐wide lncRNA microarray analysis in GBM. It showed that AC016405.3 was downregulated in GBM tissue specimens and cell lines, and it also illustrated that the downregulated AC016405.3 was closely correlated with several aggressive features of patients with GBM. Functionally, we found that overexpression of AC016405.3 suppressed GBM cells’ proliferation and metastasis using a gain of function experiment. We further showed that microRNA (miR)‐19a‐5p, a carcinogenic miRNA, was a downstream miRNA of AC016405.3. AC016405.3 was revealed as a target of miR‐19a‐5p, and overexpression of miR‐19a‐5p reversed the inhibitive effect of AC016405.3 on GBM cell proliferation and metastasis. Furthermore, a novel downstream gene of miR‐19a‐5p, TET2 , was identified through a constructed microarray analysis. We showed that TET2 was downregulated in GBM and was involved in miR‐19a‐5p‐mediated proliferation and metastasis by directly being targeted. Finally, through a western blot assay and a series of functional CCK‐8 and metastatic assays, we showed that AC016405.3 suppressed proliferation and metastasis through modulation of TET2 by sponging of miR‐19a‐5p in GBM cells. In summary, the findings of the current study identified a novel lncRNA and illustrated that AC016405.3, acting as an anti‐oncogene, suppressed GBM cell proliferation and metastasis by regulating TET through miR‐19a‐5p sponging. Our present study might provide a new axis in the molecular treatment of GBM.

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Section: Discussionmentioning

confidence: 99%

Section: Ac0164053 Suppressed Tet2-mediated Proliferation and Metamentioning

confidence: 99%

AC016405.3, a novel long noncoding RNA, acts as a tumor suppressor through modulation of TET2 by microRNA‐19a‐5p sponging in glioblastoma

Ren

2019

Cancer Science

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“…Ye et al demonstrated that TET3 demethylated the miR-30d precursor gene promoter to block TGF-β1 inducing epithelial-mesenchymal transition, thereby inhibiting ovarian cancer progression [38]. Zhu and colleagues confirmed that TET2 inhibited the carcinogensis and progression of breast tumors by regulating caspase-4 [39]. However, recent studies also revealed the tumorpromoting role of TET protein family in cancers.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic induction of tumor stemness via the lipopolysaccharide-TET3-HOXB2 signaling axis in esophageal squamous cell carcinoma

Liu

et al. 2020

Cell Commun Signal

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Background: Esophageal squamous cell cancer (ESCC) is one kind of frequent digestive tumor. The inflammatory environment plays an important role in the tumorigenesis and development of ESCC. Cancer stem cells are a small group of tumor cells with stem cell characteristics, which can potentially hinder the tumor management and treatment. Methods: ELISA was performed to detect the lipopolysaccharide concentration in cancer tissues. qPCR, Western blot, FACS, Immunohistochemistry, Immunofluorescence and Dot blot were applied to detect target genes expression. CCK-8, Colony-formation, Transwell, Sphere and Xenograft were conducted to investigate the function of cells, influenced by risk factors. The survival curve was drawn with the Kaplan-Meier product limit estimator. Nano-hmC-Seal-seq was utilized to detect the downstream target of TET3. ChIP-qPCR was adopted to demonstrate the transcriptional regulation of stem cell-associated genes by HOXB2. Results: Lipopolysaccharide concentration was significantly up-regulated in ESCC. High concentration of lipopolysaccharide stimulation induced the stemness of ESCC cells. TET3 expression was elevated with lipopolysaccharide stimulation via p38/ERK-MAPK pathway in ESCC and negatively correlated with patients' survival. TET3 induced the stemness of ESCC cells. Nano-hmC-Seal-seq showed that TET3 overexpression led to a significant increase in 5hmC levels of HOXB2 gene region, which was thus identified as the downstream target of TET3. The binding of HOXB2 to NANOG and cMYC was verified by ChIP-qPCR. Conclusions: Lipopolysaccharide served as a tumor promotor in ESCC by inducing cancer cell stemness through the activation of a LPS-TET3-HOXB2 signaling axis, which might provide a novel therapeutic strategy for ESCC.

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“…Ye et al demonstrated that TET3 demethylated the miR-30d precursor gene promoter to block TGF-β1 inducing epithelial-mesenchymal transition, thereby inhibiting ovarian cancer progression [38]. Zhu and colleagues confirmed that TET2 inhibited the carcinogensis and progression of breast tumors by regulating caspase-4 [39]. However, recent studies also revealed the tumor-promoting role of TET protein family in cancers.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic induction of tumor stemness via the Lipopolysaccharide-TET3-HOXB2 signaling axis in esophageal squamous cell carcinoma

Liu

et al. 2020

Preprint

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Background: Esophageal squamous cell cancer (ESCC) is one kind of frequent digestive tumor. The inflammatory environment plays an important role in the tumorigenesis and development of ESCC. Cancer stem cells are a small group of tumor cells with stem cell characteristics, which can potentially hinder the tumor management and treatment. Methods: ELISA was performed to detect the lipopolysaccharide concentration in cancer tissues. qPCR, Western blot, FACS, Immunohistochemistry, Immunofluorescence and Dot blot were applied to detect target genes expression. CCK-8, Colony-formation, Transwell, Sphere and Xenograft were conducted to investigate the function of cells, influenced by risk factors. The survival curve was drawn with the Kaplan-Meier product limit estimator. Nano-hmC-Seal-seq was utilized to detect the downstream target of TET3. ChIP-qPCR was adopted to demonstrate the transcriptional regulation of stem cell-associated genes by HOXB2. Results: Lipopolysaccharide concentration was significantly up-regulated in ESCC. High concentration of lipopolysaccharide stimulation induced the stemness of ESCC cells. TET3 expression was elevated with lipopolysaccharide stimulation via p38/ERK-MAPK pathway in ESCC and negatively correlated with patients’ survival. TET3 induced the stemness of ESCC cells. Nano-hmC-Seal-seq showed that TET3 overexpression led to a significant increase in 5hmC levels of HOXB2 gene region, which was thus identified as the downstream target of TET3. The binding of HOXB2 to NANOG and cMYC was veriﬁed by ChIP-qPCR. Conclusions: Lipopolysaccharide served as a tumor promotor in ESCC by inducing cancer cell stemness through the activation of a LPS-TET3-HOXB2 signaling axis, which might provide a novel therapeutic strategy for ESCC.

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Retraction Note: TET2 inhibits tumorigenesis of breast cancer cells by regulating caspase-4

Abstract: This paper has been retracted at the request of the authors.

Cited by 14 publications

References 26 publications

AC016405.3, a novel long noncoding RNA, acts as a tumor suppressor through modulation of TET2 by microRNA‐19a‐5p sponging in glioblastoma

AC016405.3, a novel long noncoding RNA, acts as a tumor suppressor through modulation of TET2 by microRNA‐19a‐5p sponging in glioblastoma

Epigenetic induction of tumor stemness via the lipopolysaccharide-TET3-HOXB2 signaling axis in esophageal squamous cell carcinoma

Epigenetic induction of tumor stemness via the Lipopolysaccharide-TET3-HOXB2 signaling axis in esophageal squamous cell carcinoma

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